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  • Plasmareninaktivität  (3)
  • Antidiuretic hormone  (2)
  • Concentrating capacity  (2)
  • Furosemide  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Rapid increase of mineralocorticoids after furosemide in low-renin essential hypertension: Evidence for 18-hydroxycorticosterone to be a better marker than aldosterone (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 847-852 
    Details
    ISSN: 1432-1440
    Keywords: Low-renin essential hypertension ; Furosemide ; Plasma renin activity ; Aldosterone ; 18-Hydroxycorticosterone ; Low-renin Hypertonie ; Furosemid ; Plasmareninaktivität ; Aldosteron ; 18-Hydroxycorticosteron
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das Verhalten der Plasmareninaktivität (PRA), des Plasmaaldosterons, des 18-Hydroxycorticosterons (18-OH-B), des 18-Hydroxydeoxycorticosterons (18-OH-DOC) und des Corticosterons wurde nach Furosemid an 20 Normalpersonen, 16 Patienten mit normal-renin Hypertonie (NREH) und 12 Patienten mit low-renin Hypertonie (LREH) untersucht. Die Blutentnahmen erfolgten unmittelbar vor der Gabe von 40 mg Furosemid i.v. sowie 15 min (im Liegen) und 120 min (aktive Orthostase) danach. Die Normalpersonen zeigten 15 min nach Furosemid einen Anstieg der PRA von 0,8±0,4 ng AI/ml·min (SD) auf 3,4±1,4 (P〈0,01), des Plasmaaldosterons von 109±28 pg/ml auf 139±40 (P〈0,01) und des 18-OH-B von 199±90 pg/ml auf 279±85 (P〈0,01). Bei Patienten mit NREH stieg die PRA signifikant geringer an (P〈0,01). Dementsprechend wurde kein signifikanter Anstieg des Plasmaaldosterons und des 18-OH-B gefunden. Bei Patienten mit LREH blieb die PRA (basal 0,2±0,1) 15 min nach Furosemid praktisch unverändert. Das Plasmaaldosteron jedoch stieg von 111±37 auf 160±66 (P〈0,05) und das 18-OH-B von 162±101 auf 261±71 an (P〈0,01). Der relative Anstieg des 18-OH-B bei Patienten mit LREH war im Vergleich zu Patienten mit NREH signifikant höher. 120 min nach Furosemid lagen die Plasmaspiegel des Aldosterons und des 18-OH-B bei Normalpersonen signifikant höher als in den beiden Patientengruppen (P〈0,01). Die Corticosteron und 18-OH-DOC Plasmaspiegel zeigten zwischen den untersuchten Gruppen kein differentes Verhalten, und es fand sich nur 120 min nach Furosemid in Kombination mit aktiver Orthostase ein signifikanter Anstieg. Die Ergebnisse zeigen, daß die Sekretion der Mineralcorticoide bei Patienten mit LREH unmittelbar nach Furosemid gesteigert ist, obwohl die PRA unverändert bleibt. 18-OH-B ist anscheinend für dieses Phänomen ein empfindlicherer Index als Aldosteron.
    Notes: Summary The response of plasma renin activity (PRA), plasma aldosterone, 18-hydroxycorticoster-one (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC) and corticosterone to furosemide were compared in 20 normal control subjects, 16 patients with normal-renin essential hypertension (NREH) and 12 patients with low-renin essential hypertension (LREH). Analyses were performed before medication, and 15 min (supine) and 120 min (active orthostasis) after IV administration of 40 mg furosemide. In normotensive subjects PRA increased 15 min after administration of furosemide from 0.8±0.4 ng AI/ml·h (SD) to 3.4±1.4 (P〈0.01), plasma aldosterone from 109±28 pg/ml to 139±40 (P〈0.01) and 18-OH-B from 199±90 to 279±85 (P〈0.01). In patients with NREH, PRA increased significantly less (P〈0.01) and no significant increase of plasma aldosterone or 18-OH-B was found. PRA of patients with LREH (0.2±0.1 ng AI/ml·h) remained practically unchanged 15 min after furosemide administration, but in contrast to NREH aldosterone increased from 111±37 to 160±66 (P〈0.05) and 18-OH-B from 162±101 to 261±71 pg/ml (P〈0.01). The relative increase of plasma 18-OH-B was significantly greater in patients with LREH than in patients with NREH. The plasma levels of aldosterone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P〈0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P〈0.01) only at 120 min after furosemide administration combined with active orthostasis. In summary, our results support the concept that sensitivity of the mineralocorticoid-producing cells is enhanced in patients with LREH. Postfurosemide 18-OH-B seems to be a better marker of this phenomenon than aldosterone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01728351
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  • 2
    Electronic Resource
    Electronic Resource
    Prostaglandin excretion after furosemide in normal and low-renin essential hypertension (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 777-782 
    Details
    ISSN: 1432-1440
    Keywords: Prostaglandins ; Furosemide ; Renin ; Potassium ; Kidney function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the urinary excretion of prostaglandin (PG)E2 and PGF2α before and 15 min after stimulation with the acutely vasodilating agent furosemide in 25 normotensive controls and 81 patients with essential hypertension (EH). After furosemide administration, PGE2 excretion was lower in patients with EH (P〈0.02). Excretion rates of PGF2α and of sodium, and urinary volume in hypertensive patients were not significantly different from the values found in normotensive controls. Patients with low-renin essential hypertension (LREH) had a significantly reduced excretion of both PGE2 and PGF2α before and after administration of furosemide as compared to controls. The difference in PGF2α excretion was also significant when LREH patients were compared to those with normal-renin essential hypertension (NREH). Patients with LREH were older and excreted less potassium than patients with NREH or normotensive controls. We conclude that the reduced PG excretion immediately after furosemide administration in patients with EH reflects a diminished capacity of the hypertensive kidney to generate prostaglandins which exert an overall vasodilating effect. Since renin secretion is under the control of renal PG formation, the decreased responsiveness of plasma renin activity (PRA) observed in patients with EH and predominantly in those with LREH may be the consequence of a decreased renal cortical PG generation. Alternatively, mechanisms that reduce both PRA and PG generation have to be considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01721777
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  • 3
    Electronic Resource
    Electronic Resource
    Individueller Verlauf des experimentellen akuten Nierenversagens: Morphologie, Funktion, Plasmareninaktivität (1974)
    Springer
    Research in experimental medicine 164 (1974), S. 203-221 
    Details
    ISSN: 1433-8580
    Keywords: Acute renal failure ; Individual course ; Renal ischemia ; Rabbit ; Histology ; Function ; Plasma renin activity ; Experimentelles akutes Nierenversagen ; Individueller Verlauf ; Renale Ischämie ; Kaninchen ; Histologie ; Funktion ; Plasmareninaktivität
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An 26 Kaninchen wurde der individuelle Verlauf des experimentellen akuten Nierenversagens (ANV) verfolgt und Änderungen der Funktion und Plasmareninaktivität den lichtmikroskopischen morphologischen Schädigungen gegenübergestellt. Trotz identischer auslösender Noxe zeigte der Einzelverlauf starke Variationen der Funktionseinschränkung, der Plasmareninaktivität und histologischer Veränderungen. Zwischen überlebenden (Gruppe A,n = 10) und urämisch sterbenden Tieren (Gruppe B,n = 16) bestand schon vom 1. postischämischen Tag an ein signifikanter Unterschied der Plasmaharnstoffkonzentration und Plasmareninaktivität (P 〈 0,01). Beide Parameter zeigten im weiteren Verlauf trotz erheblicher individueller Streuung ein für jede Gruppe charakteristisches Verhalten. Dagegen waren die morphologischen Schädigungen außerordentlich variabel und erlaubten keine Korrelation zur Einschränkung der Nierenfunktion oder dem Ausmaß der Aktivitätssteigerung des systemischen Renins.
    Notes: Summary The individual course of experimental acute renal failure (ARF) was investigated in 26 rabbits with respect to changes of renal function, plasma renin activity (PRA), and morphology. Although the cause of ARF (i.e. renal ischemia) was identical in all animals the individual course was characterized by a great variability of functional disturbance, alterations of PRA, and the degree of histological impairment. However, already on the first postischemic day a significant difference of both plasma urea concentration and plasma renin activity between group A (surviving,n = 10) and group B (non-surviving animals,n = 16) could be found, a difference that increased in significance during subsequent days of observation. In contrast the morphology was quite variabel and the degree of histological impairment could not be correlated with chance of survival, renal function, and elevation of PRA, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01852336
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  • 4
    Electronic Resource
    Electronic Resource
    Urinary cyclic AMP and renal concentrating capacity in infants (1977)
    Springer
    European journal of pediatrics 124 (1977), S. 113-119 
    Details
    ISSN: 1432-1076
    Keywords: Antidiuretic hormone ; Cyclic AMP ; Concentrating capacity ; Infant kidney
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In 15 infants between 1 and 31 weeks the effect of antidiuretic hormone (ADH) on the renal concentrating capacity and urinary cyclic AMP (cAMP) was tested. A significant decrease of urine flow and a significant increase of osmolality, urea and cAMP was observed indicating that the distal nephron of the infant kidney is responsive to exogenous ADH and that its effect is mediated by cAMP. The results of a second series with 52 normally hydrated infants demonstrate that the nonlinear age-related increase of osmolality and urea in urine is accompanied by a similar pattern of cAMP excretion, pointing out that the maturation of the concentrating capacity seems to be related to an increasing responsiveness of the cAMP system to ADH. Furthermore the results raise the possibility that increasing concentrations of urea and solutes in the medulla and papilla of the infant kidney may have—in the presence of very low ADH secretion—an additional stimulating effect on cAMP formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00477546
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  • 5
    Electronic Resource
    Electronic Resource
    Renal prostaglandins: Relationship to the development of blood pressure and concentrating capacity in pre-term and full term healthy infants (1979)
    Springer
    European journal of pediatrics 132 (1979), S. 253-259 
    Details
    ISSN: 1432-1076
    Keywords: Renal prostaglandins ; cAMP ; Blood pressure ; Concentrating capacity ; Neonatal period
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationships between urinary prostaglandins (PGs)E2 and F2α and the postnatal development of blood pressure and renal concentrating capacity were investigated in 14 pre-term and 32 full term healthy infants. Mean PGE2 and PGF2α excretion was 18.9 and 10.1 ng/h/1.73 m2, respectively, in pre-term infants. In full term infants mean urinary PGE2 was signifincantly lower (13.4 ng/h/1.73 m2) and PGF2α significantly higher (22.2 ng/h/1.73 m2). The decrease of the PGE2/PGF2α ratio (P〈0.001) was accompanied by an increase in blood pressure. High PGE2 levels in pre-term infants were inversely correlated with urinary cAMP excretion. A decreasing PGE2/PGF2α ratio in full term infants was associated with increasing urinary osmolality. After intranasal administration of antidiuretic hormone (DDAVP) in 8 full term infants the increase in urinary osmolality and cAMP excretion was accompanied by a drop in PGE2 excretion to less than half the basal values. These findings suggests that the postnatal changes in urinary PG excretion are associated with a concomittant increase in blood pressure and in the concentrating capacity of the neonatal kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00496848
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of ADH on the activity and function of the renin-angiotensin-aldosterone system in infants and in children (1976)
    Springer
    European journal of pediatrics 122 (1976), S. 303-308 
    Details
    ISSN: 1432-1076
    Keywords: Renin-angiotensin-aldosterone system ; Antidiuretic hormone ; Urinary sodium excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei Säuglingen zwischen der 1. und 25. Lebenswoche und bei Kindern zwischen dem 1. und 14. Lebensjahr wurden Renin im Plasma und Aldosteron im Urin in Abhängigkeit von der Natriumausscheidung des Endharns gemessen. Es fand sich eine reziproke Beziehung, die zeigt, daß die hohen Renin- und Aldosteronwerte der Säuglingszeit durch die niedrige Natriumaufnahme mit der Nahrung bedingt sind. Ein zusätzlicher Stimulus ist das Hypothalamus-Hypophysenhinterlappen-System, da durch antidiuretisches Hormon (ADH) Renin und Aldosteron gesenkt werden, was zu einer vermehrten Natriumausscheidung im Harn führt. Die Untersuchungen lassen eine Rückkoppelung zwischen dem Renin-Angiotensin-Aldosteron-System und der ADH-Sekretion erkennen, und diese Rückkoppelung scheint für den Wasser- und Elektrolythaushalt während der Säuglingszeit von Bedeutung zu sein.
    Notes: Abstract In babies ranging in age from 1 to 25 weeks and in children between 1 and 14 years, plasma renin activity and urinary aldosterone activity were determined in relation to urinary sodium excretion. A reciprocal correlation was found demonstrating that the hyperactivity of the renin-angiotensin-aldosterone system is stimulated in infants by a low sodium intake. A second stimulus was observed in the influence of the hypothalamo-neurohypophyseal system, when the plasma renin activity was suppressed by administration of antidiuretic hormone and sodium excretion increased due to a decreased aldosterone activity. Our study suggests that there exists a feedback between the renin-angiotensin-aldosterone system and ADH release and that this feedback plays an important role in the regulation of water and electrolyte balance in the young infant.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00481512
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  • 7
    Electronic Resource
    Electronic Resource
    Erniedrigte renale Prostaglandin E2-Ausscheidung und verminderte Stimulierbarkeit der Plasmareninaktivität bei Patienten mit essentieller Hypertonie (1979)
    Springer
    Journal of molecular medicine 57 (1979), S. 567-573 
    Details
    ISSN: 1432-1440
    Keywords: Renal prostaglandins ; Essential hypertension ; Plasma renin activity ; Renale Prostaglandine ; essentielle Hypertonie ; Plasmareninaktivität
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die renale Prostaglandin (PG)-Ausscheidung und die Stimulierbarkeit der Reninsekretion wurde bei Patienten mit essentieller Hypertonie (n=35) und bei altersgleichen normotensiven Kontrollpersonen (n=22) vergleichend untersucht. Bei den Patienten mit essentieller Hypertonie wurde eine erniedrigte basale Ausscheidung des vasodilatierenden PGE2 (p〈0,02) bei im Normbereich liegender Ausscheidung des vasokonstriktorischen PGF2α im Urin festgestellt. Darüber hinaus stieg innerhalb der ersten 15 min nach i.v.-Gabe von 40 mg Furosemid die PGE2-Ausscheidung bei Patienten mit essentieller Hypertonie signifikant geringer an als bei den Kontrollpersonen (p〈0,001), während der Anstieg der PGF2α-Ausscheidung in beiden Gruppen gleich war. Zum gleichen Zeitpunkt lag der prozentuale Anstieg der Plasmareninaktivität nach Furosemid bei Hypertonikern (167±11 (SEM)) deutlich unter dem Anstieg der Kontrollgruppe (386±46,p〈0,001). Unsere Ergebnisse unterstützen die Annahme, daß eine erniedrigte renal-kortikale, (vaskuläre?) Synthese vasodilatierender Prostaglandine die Ursache sowohl für die verminderte Stimulierbarkeit der Reninsekretion als auch für den gesteigerten renalen Gefäßwiderstand bei essentieller Hypertonie ist.
    Notes: Summary Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age-and sex-matched controls (p〈0.02). PGF2α-excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p〈0.001), while the increase in PGF2α-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167%±11, SEM) than in the normotensive (386%±46) group (p〈0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01491135
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